摘要目的 研究辛伐他汀(Sim)抑制海人酸(KA)诱导的大鼠抽搐发作向颞叶癫痫(TLE)发展的长期影响.方法 将大鼠分为健康对照组、盐水治疗癫痫组、Sim治疗癫痫组.KA诱导癫痫半小时后,Sim灌胃.(1)大鼠抽搐后3d评估了细胞因子(TNF-α、IL-1β、IL-6)的水平变化.(2)在4-6个月观察海马胶质细胞增生、神经元死亡、苔状纤维发芽(MFS)和大鼠癫痫发作情况.结果 Sim降低了TNF-α、IL-1β水平,减轻了胶质细胞增生和神经元死亡,并抑制了海马MFS和癫痫发作.结论 Sim具有抑制KA诱导的大鼠急性抽搐发作向TLE发展的效能.

abstractsObjective To examined the effect of the chronic administration of Sim immediately after epileptic seizure in rat brains with temporal lobe epilepsy (TLE).Methods (1) We evaluated cytokine expressions 3 days post KA-lesions in the hippocampus.(2) We quantified reactive astrocytosis and neuron loss in the hippocampus at 4-6 months after KA-lesions.We then assessed aberrant mossy fiber sproutings (MFS) in the epileptic brain.Seizure scores were recorded 4 to 6 months after KA-lesions.Results We found that Sim-treatment suppressed lesion-induced expressions of tumor necrosis factor-α (TNF-α)and interleukin (IL)-1β,suppressed reactive astrocytosis,and attenuated loss of neurons in the hippocampus.In contrast to the robust MFS observed in the saline-treated animals,Sim restrained the extent of MFS in epileptic rats.There was also a trend toward improvement in seizure scores.Conclusion Our study suggests that Sim administration might be a possible intervention and promising strategy for the prevention of SE intensifying to become chronic epilepsy.